Upon physiological stimulation, receptors with tyrosine kinase activity (RTK) are rapidly internalized together with their soluble ligands. T cell activation is the consequence of recognition by the T cell receptor (TCR) of specific peptide-major histocompatibility protein complexes (peptide-MHC) present at the membrane of antigen-presenting cells (APC). The TCR belongs to the RTK family and is known to be endocytosed upon ligand recognition. It differs from most other RTK in that its ligand, the peptide-MHC complex, is membrane bound and the TCR-ligand interaction is quite weak. Recent experiments have shown that the TCR ligand becomes internalized by T cells upon stimulation. Here we review current knowledge on the molecular mechanisms by which the membrane-bound MHC molecules can be transferred onto T cells, and propose hypotheses on the role this phenomenon could play in physio-pathological situations involving T cells.